Exchange diffusion and runout of Diodrast-I131 from renal tissue in vitro

Abstract

Runout of preaccumulated Diodrast-I¹³¹ from isolated goldfish kidneys was investigated with particular attention to metabolic inhibition, competition by related organic acids, and low temperature. Addition of metabolic inhibitors, such as cyanide, to medium bathing the tissue increased Diodrast runout, i.e., rate of net movement into medium. In conjunction with these same inhibitors, competitors either decreased or further increased runout, e.g., probenecid exhibited the former and p-aminohippurate (PAH) the latter action. In the absence of metabolic inhibition, increasing medium concentration of a given competitor first increased and then decreased runout. Low temperature decreased control runout as well as actions of competitors and metabolic inhibitors. Differences in lipid solubility correlate with differences in action of particular competitors. These results are interpreted as evidence for a complex membrane process mediating outward Diodrast movement, e.g., a carrier cycle which exhibits characteristics of both exchange and facilitated diffusion. Speculatively, such a process could be the basis for both active secretion and reabsorption, i.e., bidirectional tubular transport of organic acids.